FINAL Flashcards

1
Q

Gastroesophageal Reflux Disease (GERD) Patho

A

Weak, lower esophageal sphincter tone allows reflux of acid pepsin into esophagus

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2
Q

Risk Factors for GERD

A
  • Age
  • High BMI
  • Smoking
  • Large meals
  • Acidic foods, caffeine, alcohol
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3
Q

Causes of Peptic Ulcer Disease (PUD)

A
  • H. Pylori bacteria (bacterial infection in stomach)
  • Alcohol
  • NSAIDs (non-steroidal anti-inflamm drugs)
  • Smoking
  • Medications
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4
Q

Diverticulitis Patho

A

Infected diverticulum pouch = inflammation

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5
Q

CMs of Diverticulitis

A
  • Cramping & abdominal pain (in LLQ)
  • Diarrhea, constipation, distention, flatulence
  • Fever, leukocytosis
  • N/V
  • Diverticular hemorrhage: melena (dark stools from blood), rectal bleeding
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6
Q

Diverticulosis vs Diverticulitis

A

-litis = inflammed pouches; infection
-losis = development of abnormal pouches; asymptomatic

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7
Q

Ulcerative Colitis

A
  • Chronic ulceration
  • Affects inner most lining (mucosa) of the large colon & rectum
  • Continuous; no skipped lesions
  • Stools = bloody & mucous
  • Abdominal cramping
  • Incrd risk for colon cancer
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8
Q

Crohn’s Disease

A
  • Chronic, relapsing
  • Can affect any part of GI tract from mouth to anus of the entire thickness
  • Discontinuous; skipped lesions
  • Cobblestone appearance
  • Abdominal pain
  • Diarrhea w/ or w/out blood
  • Anemia from malabsorption
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9
Q

Complications of Lower GI Disorders

A
  • Fistula: abnormal opening/pathway of 2 surfaces tht aren’t suppose to touch
  • Abscess: collection of infection under skin
  • Perforation w/ peritonitis: a hole tht develops in wall of organ tht becomes inflammed
  • Necrotic bowel
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10
Q

Portal Hypertension Patho

A

Localized pressure in portal veins (of liver) is high due to scarring of the liver causing blood to not go back to heart resulting in accumulation of blood = HTN
(high BP in portal venous system; >10mmHg)

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11
Q

CM for Portal HTN

A
  • Esophageal varices
  • Ascites
  • Splenomegaly
  • Hepatic Encephalopathy
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12
Q

Cirrhosis Patho

A
  • End stage liver disease
  • Functional liver replaced by fibrosis & scarring
  • Constrictive bands disrupt flow of blood vessels & biliary ducts
    >leads to portal HTN bc blood is not metabolize
    >leads to bile stasis from obstruction of biliary channels = death of liver cells & liver failure
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13
Q

Causes of Cirrhosis

A
  • Alcohol
  • Viral hepatitis
  • Autoimmune
  • Primary & secondary biliary cirrhosis (destructive of bile ducts)
  • Nonalcoholic fatty liver disease
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14
Q

Causes of Jaundice

A
  1. Excessive destruction of RBCs
  2. Impaired uptake of bilirubin by liver cells
  3. Drcd conjugation of bilirubin
  4. Obstruction of bile flow
  5. Excessive extrahepatic production of bilirubin
    (basically cirrhosis?)
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15
Q

Jaundice Patho

A

Fibrotic liver cells are unable to uptake bilirubin, metabolize bilirubin, and excrete bilirubin in bile

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16
Q

Hepatitis Prevention

A
  • Hep A: hand-washing (fectal-oral route)
  • Hep C: avoid shared needles & blood of someone else infected
    (most common reason for liver transplant)
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17
Q

Hepatitis CMs + Phases

A
  1. Prodromal / Pre-icterus
    >abrupt to insidious: malaise, myalgia, fatigue, anorexia, N/V, diarrhea, abdominal pain, fever chills; serum lvls of AST & ALT incr
  2. Icterus (jaudice); 7-14 days laters
    >jaundice, pruritus, liver tenderness, rise in serum bilirubin
  3. Recovery; complete recovery 1-4 mnths
    >jaundice disappears, return to normal
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18
Q

Lab Values of Liver Dysfunction

A
  • Liver enzymes: high
    >aspartate transaminase (AST): highest in hepatitis/cancers
    >alanine transaminase (ALT): specific to liver inflamm
    >alkaline phosphatase (ALP): liver disease; bile obstruction
  • Bilirubin: high
  • Prothrombin Time (bleeding): prolonged; liver isn’s synthesizing clotting factors & vit K
  • Ammonia: high
  • Albumin: low
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19
Q

Substances of Gallstones

A
  • Cholesterol
  • Biliary salts
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20
Q

Causes of Cholecystitis

A
  • Calculous (90%): obstruction by stones = inflammation
  • Acalculous (10%): infection/sepsis or trauma; no stones
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21
Q

Pancreatitis Patho

A
  • Autodigestion (pancreas digesting itself) of tissue by abnormal activation of pancreatic enzymes (trypsin)
  • Inflammatory response
  • Incrd vascular permeability leads to hemorrhage, edema, & necrosis
    >mild to severe symptoms
    >may progress to multi-organ failure
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22
Q

Why NPO for Pancreatitis

A

Signal to pancreas to produce enzymes is not activated

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23
Q

Type I Diabetes

A
  • No insulin secretion
  • Autoimmune/idiopathic
  • Destruction of beta-cells
  • Cannot modify risk
  • Peak age: 12-14yrs
  • DKA if CM not caught in time
  • CM: polyuria, polydipsia, polyphagia
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24
Q

Type II Diabetes

A
  • Some functional insulin
  • Defect insulin receptors
  • Incrd insulin resistance
  • Can modify some risk to prevent or delay onset
  • Peak age > 40yrs
  • Complications at diagnosis
  • CMs: 3 Ps, blurred vision/retinopathy, paresthesia/PVD, fatigue, frequent infections, wounds slow healing, candida (yeast) infections
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25
Hypoglycemia
- Blood glucose >50 mg/dL - Caused by too much medication, too little food, or excess physical exercise: treat before loss of consciousness - CM: >cool, clammy skin >anxiety, hunger, tachycardia, tremors >fatigue, confusion, headache, dizziness >seizures, coma, death
26
Complications of Wound Healing
- Dehiscence: wound separates - Evisceration: total separation of wound layer, protrusion of organs - Fistula: abnormal passage btwn 2 organs or to outside of body - Osteomyelitis: infection of bone
27
Normal Wound Healing
- Goals: fill in, seal, & shrink wound - Primary Intention: minimal tissue loss, wound edges approximated, little epithelization & shrinkage, low risk infection
28
Types of Bowel Obstruction
- Non-mechanical: failure of normal motility (postop & narcotics) - Mechanical: >adhesions: scarring/strictures >hernia: protrusion through abd wall >intusseption: (telescope) part of intestine slides into adjacent part >torsion: complete twisting (vovulus) >cancer
29
CMs of Bowel Obstructions
- N/V - Constipation or diarrhea - Abd pain/distention - Hyper/hypoactive sounds RED FLAGS: - abrupt severe pain - guarding - tachycardia - fever - bloody stool (could be perforation)
30
Esophageal Varices
- Back pressure causes vessel varices (bleeding) - CMs: bleeding/hematemesis, rupture possible
31
Ascites
- Incr in amnt of fluid in peritoneal cavity - Imapired albumin synthesis; fluid loss out vascular space, low BP - Inability to metabolize aldosterone; salt & water retention - Fluid imbalance self perpetuating
32
Splenomegaly
- Spleen enlarges due to PHTN shunting blood into splenic vein - Hypersplenism develops: dcrd lifespan of RBCs, WBCs, & platelets - CM: anemia, bleeding, infections
33
Hepatic Encephalopathy
- Liver lost its detoxifying capacity; high blood ammonia lvls circulates brain - CMs: neural disturbances; confusion/disorientation, asterixis - flapping tremor - early, memory loss/personality changes (euphoria, irritability, anxiety), impaired speech, progresses to deep coma
34
Labs for Diabetes
- HbA1c avg of blood glucose levels over 3 months - Fasting Blood Glucose
35
Neuropathy
- Chronic complication to microvascular vessels secondary to hyperglycemia - Damage to myelin sheath (sensory) >loss of sensation, pain/paresthesia, injuries/foot ulcers >autonomic neuropathy: end organ damage
36
Retinopathy
- Blindness - Dcrd blood flow to retina = ischemia, body attempts to repair, leads to scarring, then repeats
37
Nephropathy
- Damage to glomerulus, causes scarring = loss of function - Progressive renal insufficiency/failure
38
Foot Ulcer/Diabetic Ulcer
Low blood profusion and loss of sensation of lower extremities (peripheral neuropathy) can cause injuries and ulcers
39
Natural-Active Immunity
- Human body is reacting to something - EX: building antibodies after getting cold - Cold was already existing, but body MADE memory cells to fight off antigen
40
Acute Inflammatory Response
- Injury to vascularized tissue will activate IR - Goal: limit extent of tissue damage, destroy microorganism, initiate adaptive IR, begin healing - CM: HELPR - EX: infection, necrosis, nutrient deprivation, genetic or immune defects, chemical injury, foreign bodies, temperature extremes, ionizing radiation
41
Natural-Passive Immunity
- Not doing anything, passively receiving - EX: if mother is sick and makes antibodies and passes antibodies to fetus in womb - Immunity was not made in a lab, baby did nothing to receive antibodies
42
P in HELPR
PAIN - Mediator will stimulate the nerve ending, causing pain
43
L in HELPR
LOSS OF FUNCTION Due to swelling, can cause joints or affected area to lose their function
44
R in HELPR
REDNESS Due to vasodilation from increased RBC blood flow
45
H in HELPR
HEAT - Caused by vasodilation from histamine release - Heat happens because of increased blood flow
46
E in HELPR
EDEMA SWELLING happens bc vascular permeability increases, causing fluids to come out of the vessels and accumulate in the inflamed area
47
Malignant Tumor Cells
- D not look like normal cells - Do not perform normal cell functions - Lack capsules, look like a crap trying to filtrate surrounding tissue - Grow rapidly, forming "new tissue" - Don't die (no apoptosis) to keep cell count constant - Cause destruction & metastasize
48
2nd Stage of Wound Healing
- Proliferation and new tissue formation : 3 days - 2 weeks - Granulation tissue grows (2nd step) into wound surrounding healthy tissue - Granulation happens bc of angiogenesis (1st step); forms new capillaries - Re-epithelialization (3rd step); skin reformation across wound bed
49
1st Stage of Wound Healing
Inflammation : 1-3 days
50
3rd Stage of Wound Healing
- Remodeling and Maturation : 3 weeks - >6 months - Tissue regeneration, wound contraction continue = scar tissue formation
51
Pressure Ulcer
- Pressure + time = tissue death - Soft tissue compression btwn bony prominence & external surface, pressure exceeds capillary filling pressure
52
Anemia
- A clinical manifestation, not a specific disease - Labs: dcr Hgb, Hct, & RBC - Diminished O2 - Fatigue, weakness, activity intolerance, pallor, cool extremities, exertional dyspnea, rapid HR
53
Iron Deficiency Anemia
- Most common - Deficient iron = dcr Hgb production = impaired O2 delivery - Common causes: chronic blood loss (GI bleed, heavy period), poor GI absorption of iron, poor diet
54
Blood Loss Anemia
- Acute: rapid hemorrhage (surgery, trauma), loss of intravascular volume (poor delivery of O2), circulatory collapse (hypotension, tachycardia) - Chronic: slow bleed (GI, menstrual disorders), does not affect blood volume (leads to iron-def anemia bc production can't keep up, depleted iron storage)
55
Megaloblastic Anemia
- Deficiencies of folic acid, B12, and/or intrinsic factor - Folic acid: required for DNA synthesis of normal RBC - B12: required to move folic acid into cells - Intrinsic Factor: secreted by parietal cells of gastric mucosa, required for B12 absorption, lack causes pernicious anemia
56
Pernicious Anemia
- Lack of parietal cells, unable to excrete intrinsic factor, failure to absorb B12 - Cause: atrophic gastritis, autoimmune destruction of gastric mucosa - CMs: moderate to severe anemia CMs, demyelination spinal cord causes symmetry paresthesias of feet/fingers, loss of vibratory & position sense, confusion, dementia
57
Hemolytic Anemia
- Inherited disorder of abnormal Hgb - Dcrd O2 cause distortion of RBC shape (sickle cell); early death of RBC (hemolytic), sickled RBCs stick together & occlude small vessels
58
Erythropoiesis, Erythropoietin
- Erythropoiesis is driven by tissue O2 needs - Dcr in O2 to tissues is detected by kidneys; kidneys produce erythropoietin (hormone); erythropoietin stimulates production of pro-erythroblasts from stem cells in bone marrow - RBC self destructs as it squeezes through spaces of spleen or phagocytic macrophages ingest & destroy RBCs - Heme unit is converted to bilirubin in liver; secreted in bile, feces, & urine - Rate destruction = rate production (normally)
59
Atherosclerosis
- Progressive disease - Associated w/ dyslipidemia - Patho: >injury to endothemlium & tunica intima (inflamm process) by risk factors >foam cells: LDL chol invades tunica intima layer, macrophages "eat up" LDL & die accumulating & building fatty layers (streaks) >plaque structure: smooth muscle cells of tunica media form fibrous capsule of collagen & elastin over fatty streaks & lay down Ca deposits, plaque build up is a repetitive process >artery lumen narrows: ischemia, effects on body depends on structures involved & extent of altered flow, infarction can occur when plaques dislodge
60
Plaques
- Stable: obstruct flow = little O2, less dangerous - Unstable: plaque rupture & migration through vessel, more dangerous
61
Peripheral Artery Disease (PAD)
- Progressive disease, atherosclerosis narrows arteries in legs & feet; dcrd blood flow - CMs: claudication pain, thinning skin, pulse poor/absent, skin cool, ulcers (pale, dry, punched out), surrouding skin dry & shiny, dcrd perfusion, dependent rubor - Comps: rest pain, ulcers, gangrene, amputation - Tx: stent, bypass graft
62
Acute Peripheral Artery Occlusion
- Complication of an unstable clot, not progressive - Unstable plaque or clot obstructs artery; lack of blood supply to extremity results in tissue death in hrs - CMs: sudden onset 7 Ps - Tx: thrombolytic therapy, embolectomy
63
Chronic Angina
- Coronary artery disease or MI - Atherosclerosis - Angina = chest pain - Intermittent imbalance btwn coronary blood flow & metabolic demands of myocardium - Chest pain, SOA, relieved by rest & nitro - Precipitated by: physical exertion, exposure to cold, emotional stress
64
Right Ventricular Failure (HF)
- Causes: L side ventricular dysfunction, cor pulmonale (COPD), pulmonary HTN, valve dysfunction (tri or pulm) - Reduced blood flow into pulmonary circulation & L side heart, dcrd CO, incrd pressure of RV/RA/systemic venous system - End Result: congestion of peripheral tissue - CMs: congestion of periph tissues; periph edem = fluid weight gain, liver congestion = impaired liver function, GI congestion = anorexia/tissue wasting & GI distress - SWELLING: swelling (legs, liver, GI), weight gain (fluid, rapid), edema (pitting), large neck vein (JVD), lethargy, irregular HR, nocturia, girth (ascites)
65
Aortic Valve Stenosis
- Aortic valve is btwn LV & aorta - Hardening of valve - Incomplete opening; incrd resistance to ejection of blood from LV into aorta; maintains EF until valve 1/4 normal size - Compensatory mech: LV hypertrophy - Comp: LV HF - Causes: age-related calcification, congenital malformation CMs: murmur syncope, LHF
66
Deep Vein Thrombus (DVT)
- DVT: injury to vessels occurs, inflamm response/clotting cascade initiated = thrombus grows in direction of blood flow - CMS: unilateral swelling, pain/tenderness, warmth, redness
67
Pulmonary Embolism (PE)
- Risk Factors: Virchow's triad (venous stasis, coagulability, endothelial injury) - Effects depends on extent of blood flow obstruction, size of vessels, secondary effects (infarction) - Result: embolism w/ infarction or w/out, massive occlusion, multiple occlusions - CMs: small; intermittent SOA, exercise intolerance. large; sudden onset, severe chest pain, respiratory distress/acute hypoxemia, loss of consciousness, shock (rapid, weak pulse, hypotension, diaphoresis) - Dx: V/Q scan, CT scan, ABG
68
Chronic Obstructive Pulmonary Disease (COPD)
- Inflamm & destruction of lung parenchyma/central airways causing irreversible expiratory limit - Smoking is biggest cause - Combo of chronic bronchitis & emphysema - CMs: early; cough (excessive mucus_, incrd RR, exercise dyspnea, wheezing. late; constant dyspnea, trapped air, prolonged expiration, barrel chest & use of accessory muscles, cyanosis, clubbing of fingers, pulmonary HTN/ R HF - Comps: R HF
69
Chronic Bronchitis
- Excessive mucus production, mucus plugging, & fibrosis - Hypoxia/hypercapnia, shunting, pulm HTN, cor pulmonale - Shunting = vasoconstriction everywhere in lungs (no good place) = puml HTN - Inflamm response is consistent bc irritation is consistent - Mucus production id from vascular perm - Blue bloater
70
Emphysema
- Abnormal permanent enlargement & destruction of air spaces distal to terminal bronchioles, loss of elasticity - Collapse during expiration, air trapping, CO2 retention (hypercapnia) - Pink puffer
71
Pneumonia
- Infection/inflamm causes excess fluid & edema = poor gas exchange - Classified according to source: community acquired or hospital acquired - Risk Factors: recent exposure, tobacco/substance use, chronic lung disease, aspiration risk, mechanical ventilation, immune compromise, age, atelectasis - Dx: elevated WBC, sputum C & S, ABGs, CXR - CMs: early; malaise, fever, severe shaking/chills, fine crackles. progression; purulent sputum, pleuritic chest pain, resp distress/acute hypoxemia
72
Fractures
- Injury, stress fracture (incomplete crack), pathologic fracture (underlying cause) - At risk for: bleeding, circulation & neurologic impairment due to pressure, loss of function, infection - Types: open/compound vs closed, complete vs incomplete, comminuted (2+ pieces), impacted (2 wedged), compression (2 crushed), transverse (across bone perpendicular) - CMs: pain, swelling, loss of function/mobility, crepitus or grating as bone fragments rub together, deformity (angulation, shortening, rotation) - Tx: reduction, immobilization, prevention of complication & restoration of function
73
Fractures Healing & Complications
- 24-72hrs: hematoma - 3-14 days: granulation tissue (soft tissue callus) - 4-6 wks or a yr: remodeling - Comps: impaired healing due to age, inadequate circulation, coagulation disorders, DM, poor nutrition
74
Osteomylitis
- Bloodstream (hematogenous), direct penetration, contamination of open wound - Bones destruction/abscess, exudate infiltrates, periosteum, blood supply to bone cortex destroyed = necrosis - CMs: symptoms of bacteremia & local site infection; chills, fever, malaise, edema, erythema, drainage, pain - Tx: longterm antibiotics, surgery debridement
75
Compartment Syndrome
- Dcr in compartment size (constrictive casts, dressings, etc.) - Incr in compartment volume (bleeding, inflamm) - Compromises circulation, death to nerve & muscle cells, permanent loss of function, symptoms begin w/in hrs, muscle necrosis in 4-8hrs - CMs: pain, parathesia, pallor, pulselessness, poikilothermic, paralysis - Tx: notify HCP - Goal: reduce pressure
76
CKD Labs
- GFR: dcrd - BUN: elevated (incrd nitrogen) - Surem Creatinine: elevated - Urine Protein: elevated (leads to swelling, microalbuminuria is 1st symp of CKD) - Anemia: dcrd RBC & Hgb (kidneys don't release erythro) - Hyperparathyroidism: dcr vit D & Ca, incr P (kidneys don't excrete P, P & Ca have inverse relationship, kidneys not converting vit D to calcitriol bc of impaired absorption of Ca)
77
Acute Kidney Injury
Abrupt decline in kidney function results in inability to maintain F&E balance and excrete nitrogenous waste
78
Prerenal
- Dcrd blood flow w/out ischemia injury - Hypovolemia: hemorrhage, dehydration, shock - Hypotension: poor perfusion
79
Intrarenal
- Conditions tht damage renal structures - Ischemia: glomerulonephritis, pyelonephritis, sepsis, toxins from massive infections, nephrotoxic meds
80
Postrenal
- Urine outflow blocked - Bilateral ureteral obstruction, bladder obstruction (BPH, tumor), stones
81
Renal Labs
- GFR estimates how much blood passes through the glomeruli each minute; incrd w/ age & men (musc mass) - Urinalysis - Creatinine: product of muscle metabolism, reflects GFR, renal damage: urine level dcr, blood lvl incr, alos incrd during trauma/breakdown of muscle tissue - BUN: urea made in liver during protein breakdown, reflects GFR & urine concentration ability, incrd when GFR is dcrd, incrd in dehydration, dcrd in fluid excess
82
Brain Herniation
- Incrd ICP: blood, brain tissue, CSF - Interferes w/ perfusion - Risk Factors: hemorrhage (brain bleed, CVA), brain tumor, hydrocephalus (excess CSF) - Early CMs: changed/dcrd LOC (restless, irritable, confusion, drowsiness), headahce, pupils small & sluggish - Late CMs: worsening tissue hypoxia (lethargy, stupor, coma) HTN, bradycardia, abnormal resp patterns, unilateral large & unreactive pupil - Comps: displacement of brain tissue from area of high pressure to low pressure, pressure placed on brainstem; control lost (CV & resp), lateral pressure compressed CN III
83
Post Concussion Syndrome
- Lasts days to months, can last yrs - Persistent headahce, dizziness, attention deficits, irritability, insomnia, impaired judgement, anxiety/depression
84
Tonic-Clonic Seizures
- Tonic phase: immediate loss of consciousness, sharp tonic contractions of musc w/ extension of extrems, incontinence of bowel/bladder, cyanosis if airway compromised - Clonic Phase: rhythmic bilateral contraction & relaxation of extrems
85
Postictal State
- Recovery period - 5-30 mins - Unconscousness/deep sleep, headache, confusion, dysphagia, mem loss, HTN